Archive for the ‘Gene Therapy Research’ Category
Discovery of a gene that causes Joubert Syndrome
Public release date: 10-May-2012 [ | E-mail | Share ]
Contact: William Raillant-Clark w.raillant-clark@umontreal.ca 514-343-7593 University of Montreal
This press release is available in French.
C5ORF42 was identified as the gene that causes Joubert Syndrome in a number of families in the Lower St. Lawrence region of Quebec where the causal gene had remained unknown since the initial description of the syndrome in 1969. This is what a study in the April issue of The American Journal of Human Genetics reveals. The study was conducted by researchers from the Sainte-Justine University Hospital Research Center and the Centre of Excellence in Neuromics of Universit de Montral (CENUM).
Joubert Syndrome is a condition that affects brain development and manifests itself through delayed psychomotor development, abnormal coordination of eye movements and respiratory abnormalities. Since Dr. Marie Joubert and her colleagues described it for the first time in 1969, a number of related genes have been identified in various populations, but the causal gene of the Quebec form of the syndrome has remained until now unknown.
"No studies had been done to identify the genetic origin of the disease in Quebec, more specifically in the exact area of the Lower St. Lawrence where most cases in Quebec are concentrated," Dr. Jacques Michaud, the study's principal investigator, explained. "This is the first study to present a picture of Joubert syndrome in the Quebec population. It will allow family members affected by the syndrome to assess their children's genetic risks with a simple DNA test."
The finding is interesting, both genetically and historically, since, while Joubert Syndrome is present around the world, genetic strains can vary regionally. Distribution is related to the history of various population groups.
Quebec is no exception. In fact, 6,000 French Canadian settlers from Quebec City and its surroundings settled in the Lower St. Lawrence region about the end of the 17th and beginning of the 18th centuries. The fact that most present day inhabitants of the Lower St. Lawrence region descend from this small group of settlers suggests a genetic founder effects. Indeed, certain founder mutations are transmitted to a large number of descendants, which increases the risk of genetic diseases in offspring.
As a matter of fact, Dr. Michaud's team identified three C5ORF42 mutations that are common to most of the families in the study. In all, seven families that are carriers of the gene were identified in a 400-km area along Route 132.
In the space of about two centuries, the first colonists settled in the Lower St. Lawrence region and from there other families headed out to settle along the river heading east as far as Mont-Joli and then along the Matapedia River. According to Myriam Srour, a doctoral student and co-author of the study, the mutations likely spread in the population along these migration routes.
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Discovery of a gene that causes Joubert Syndrome
Transplanted Gene-Modified Blood Stem Cells Protect Brain Cancer Patients From Toxic Side Effects of Chemotherapy
Study is first to show feasibility and efficacy of a new use for autologous stem cell transplant
Newswise SEATTLE For the first time, scientists at Fred Hutchinson Cancer Research Center have transplanted brain cancer patients own gene-modified blood stem cells in order to protect their bone marrow against the toxic side effects of chemotherapy. Initial results of the ongoing, small clinical trial of three patients with glioblastoma showed that two patients survived longer than predicted if they had not been given the transplants, and a third patient remains alive with no disease progression almost three years after treatment.
We found that patients were able to tolerate the chemotherapy better and without negative side effects after transplantation of the gene-modified stem cells than patients in previous studies who received the same type of chemotherapy without a transplant of gene-modified stem cells, said Hans-Peter Kiem, M.D., senior and corresponding author of the study published in the May 9 issue of Science Translational Medicine.
Kiem, a member of the Clinical Research Division at the Hutchinson Center, said that a major barrier to effective use of chemotherapy to treat cancers like glioblastoma has been the toxicity of chemotherapy drugs to other organs, primarily bone marrow. This results in decreased blood cell counts, increased susceptibility to infections and other side effects. Discontinuing or delaying treatment or reducing the chemotherapy dose is generally required, but that often results in less effective treatment.
In the current study, Kiem and colleagues focused on patients with glioblastoma, an invariably fatal cancer. Many of these patients have a gene called MGMT (O6-methylguanine-DNA-methyltransferase) that is turned on because the promoter for this gene is unmethylated. MGMT is a DNA repair enzyme that counteracts the toxic effect of some chemotherapy agents like temozolomide. Patients with such an unmethylated promoter status have a particularly poor prognosis.
A drug called benzylguanine can block the MGMT gene and make tumor cells sensitive to chemotherapy again, but when given with chemotherapy, the toxic effects of this combination are too much for bone marrow cells, which results in marrow suppression.
By giving bone marrow stem cells P140K, which is a modified version of MGMT, those cells are protected from the toxic effects of benzylguanine and chemotherapy, while the tumor cells are still sensitive to chemotherapy. P140K can repair the damage caused by chemotherapy and is impervious to the effects of benzylguanine, Kiem said.
This therapy is analogous to firing at both tumor cells and bone marrow cells, but giving the bone marrow cells protective shields while the tumor cells are unshielded, said Jennifer Adair, Ph.D., who shares first authorship of the study with Brian Beard, Ph.D., both members of Kiems lab.
The three patients in this study survived an average of 22 months after receiving transplants of their own circulating blood stem cells. One, an Alaskan man, remains alive 34 months after treatment. Median survival for patients with this type of high-risk glioblastoma without a transplant is just over a year.
Glioblastoma remains one of the most devastating cancers with a median survival of only 12 to 15 months for patients with unmethylated MGMT, said Maciej Mrugala, M.D., the lead neuro oncologist for this study.
Gene-modified stem cell transplant protects patients from toxic side effects of chemotherapy
Public release date: 9-May-2012 [ | E-mail | Share ]
Contact: Dean Forbes dforbes@fhcrc.org 206-667-2896 Fred Hutchinson Cancer Research Center
SEATTLE For the first time, scientists at Fred Hutchinson Cancer Research Center have transplanted brain cancer patients' own gene-modified blood stem cells in order to protect their bone marrow against the toxic side effects of chemotherapy. Initial results of the ongoing, small clinical trial of three patients with glioblastoma showed that two patients survived longer than predicted if they had not been given the transplants, and a third patient remains alive with no disease progression almost three years after treatment.
"We found that patients were able to tolerate the chemotherapy better and without negative side effects after transplantation of the gene-modified stem cells than patients in previous studies who received the same type of chemotherapy without a transplant of gene-modified stem cells," said Hans-Peter Kiem, M.D., senior and corresponding author of the study published in the May 9 issue of Science Translational Medicine.
Kiem, a member of the Clinical Research Division at the Hutchinson Center, said that a major barrier to effective use of chemotherapy to treat cancers like glioblastoma has been the toxicity of chemotherapy drugs to other organs, primarily bone marrow. This results in decreased blood cell counts, increased susceptibility to infections and other side effects. Discontinuing or delaying treatment or reducing the chemotherapy dose is generally required, but that often results in less effective treatment.
In the current study, Kiem and colleagues focused on patients with glioblastoma, an invariably fatal cancer. Many of these patients have a gene called MGMT (O6-methylguanine-DNA-methyltransferase) that is turned on because the promoter for this gene is unmethylated. MGMT is a DNA repair enzyme that counteracts the toxic effect of some chemotherapy agents like temozolomide. Patients with such an unmethylated promoter status have a particularly poor prognosis.
A drug called benzylguanine can block the MGMT gene and make tumor cells sensitive to chemotherapy again, but when given with chemotherapy, the toxic effects of this combination are too much for bone marrow cells, which results in marrow suppression.
By giving bone marrow stem cells P140K, which is a modified version of MGMT, those cells are protected from the toxic effects of benzylguanine and chemotherapy, while the tumor cells are still sensitive to chemotherapy. "P140K can repair the damage caused by chemotherapy and is impervious to the effects of benzylguanine," Kiem said.
"This therapy is analogous to firing at both tumor cells and bone marrow cells, but giving the bone marrow cells protective shields while the tumor cells are unshielded," said Jennifer Adair, Ph.D., who shares first authorship of the study with Brian Beard, Ph.D., both members of Kiem's lab.
The three patients in this study survived an average of 22 months after receiving transplants of their own circulating blood stem cells. One, an Alaskan man, remains alive 34 months after treatment. Median survival for patients with this type of high-risk glioblastoma without a transplant is just over a year.
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Gene-modified stem cell transplant protects patients from toxic side effects of chemotherapy
Can new diagnostic approaches help assess brain function in unconscious, brain-injured patients?
Public release date: 9-May-2012 [ | E-mail | Share ]
Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News
New Rochelle, NY, May 9, 2012Disorders of consciousness such as coma or a vegetative state caused by severe brain injury are poorly understood and their diagnosis has relied mainly on patient responses and measures of brain activity. However, new functional and imaging-based diagnostic tests that measure communication and signaling between different brain regions may provide valuable information about the potential for consciousness in patients unable to communicate. These innovative approaches are described and compared in a Review article in the groundbreaking neuroscience journal Brain Connectivity, a bimonthly peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Brain Connectivity website at http://www.liebertpub.com/brain.
Mlanie Boly and coauthors from University of Lige (Belgium), University of Milan (Italy), and University College London (UK) compare the benefits and limitations of three methods for studying the dynamics of brain communication and connectivity in response to internal and external stimulation: functional magnetic resonance imaging f(MRI); transcranial magnetic stimulation (TMS) combined with electroencephalograpy (EEG); and response to neuronal perturbation, measuring, for example, sensory evoked potentials (ERP). They report their findings and propose future research directions in the article "Brain Connectivity in Disorders of Consciousness."
"In recent years, there has been a tremendous interest in gaining a better understanding of the various disorders of consciousness. A variety of methods including fMRI and PET have been used to study these disorders," says Bharat Biswal, PhD, Co-Editor-in-Chief of Brain Connectivity and Associate Professor, University of Medicine and Dentistry of New Jersey. "This article provides a comprehensive analysis using three new and innovative methods to study disorders of consciousness."
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About the Journal
Brain Connectivity is the journal of record for researchers and clinicians interested in all aspects of brain connectivity. The Journal is under the leadership of Founding and Co-Editors-in-Chief Christopher Pawela, PhD, Assistant Professor, Medical College of Wisconsin, and Bharat Biswal, PhD. It includes original peer-reviewed papers, review articles, point-counterpoint discussions on controversies in the field, and a product/technology review section. To ensure that scientific findings are rapidly disseminated, articles are published Instant Online within 72 hours of acceptance, with fully typeset, fast-track publication within 4 weeks. Tables of content and a sample issue may be viewed on the Brain Connectivity website at http://www.liebertpub.com/brain.
About the Publisher
Mary Ann Liebert, Inc. is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Tissue Engineering, Human Gene Therapy and HGT Methods, and Rejuvenation Research. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, newsmagazines, and books is available on the Mary Ann Liebert, Inc. website at http://www.liebertpub.com.
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Can new diagnostic approaches help assess brain function in unconscious, brain-injured patients?
Genetic packing: Successful stem cell differentiation requires DNA compaction, study finds
Hematoxylin and eosin (H&E) staining of sections of wild-type (top row) and H1 triple-knockout (bottom row) embryoid bodies. After 14 days in rotary suspension culture, the wild-type embryoid bodies showed more differentiated morphologies with cysts forming (black arrows) and the knockout embryoid bodies failed to form cavities (far right). (Credit: Yuhong Fan)
(Phys.org) -- New research findings show that embryonic stem cells unable to fully compact the DNA inside them cannot complete their primary task: differentiation into specific cell types that give rise to the various types of tissues and structures in the body.
Researchers from the Georgia Institute of Technology and Emory University found that chromatin compaction is required for proper embryonic stem cell differentiation to occur. Chromatin, which is composed of histone proteins and DNA, packages DNA into a smaller volume so that it fits inside a cell.
A study published on May 10, 2012 in the journal PLoS Genetics found that embryonic stem cells lacking several histone H1 subtypes and exhibiting reduced chromatin compaction suffered from impaired differentiation under multiple scenarios and demonstrated inefficiency in silencing genes that must be suppressed to induce differentiation.
While researchers have observed that embryonic stem cells exhibit a relaxed, open chromatin structure and differentiated cells exhibit a compact chromatin structure, our study is the first to show that this compaction is not a mere consequence of the differentiation process but is instead a necessity for differentiation to proceed normally, said Yuhong Fan, an assistant professor in the Georgia Tech School of Biology.
Fan and Todd McDevitt, an associate professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University, led the study with assistance from Georgia Tech graduate students Yunzhe Zhang and Kaixiang Cao, research technician Marissa Cooke, and postdoctoral fellow Shiraj Panjwani.
The work was supported by the National Institutes of Healths National Institute of General Medical Sciences (NIGMS), the National Science Foundation, a Georgia Cancer Coalition Distinguished Scholar Award, and a Johnson & Johnson/Georgia Tech Healthcare Innovation Award.
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Phase contrast images showing that H1 triple-knockout (bottom) embryonic stem cells were unable to adequately form neurites and neural networks compared to wild-type embryonic stem cells (top). (Click image for high-resolution version. Credit: Yuhong Fan)
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Genetic packing: Successful stem cell differentiation requires DNA compaction, study finds
Genetic predictor of breast cancer response to chemotherapy
Public release date: 10-May-2012 [ | E-mail | Share ]
Contact: Dr. Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central
Chemotherapy is a major first line defense against breast cancer. However a patient's response is often variable and unpredictable. A study published in BioMed Central's open access journal BMC Medical Genomics shows that 'gene expression signatures' for TOP2A and -tubulin can be used to predict the outcome of chemotherapy.
The goal of personalized medicine in cancer treatment is to target therapy to the characteristics of the individual tumor. For example Herceptin treatment is of most benefit to patients whose cancer is driven by HER2 and antiestrogens benefit patients whose breast cancer is hormonally driven. Gene signatures are increasingly available for different cancer types and can be used to predict patient prognosis.
Researchers from McMaster University, in association with the Juravinski Hospital and Cancer Center, analyzed the expression of the enzyme TOP2A (DNA topoisomerase) and -tubulin, which are the targets of commonly used chemotherapy drugs (anthracycline and taxane) in hundreds of breast tumors. Combining the results from the tumor samples analyses allowed the researchers to build gene expression 'signatures' that measure the susceptibility of tumor cells to chemotherapy.
Both of the 'signatures' were separately able to predict which patients achieved a complete response (where invasive or metastatic cancer could no longer be detected) and together the two indices together were even more accurate at predicting response to chemotherapy.
Prof John Hassell, who led this study, commented, " Our results clearly demonstrate the practicality of using gene expression to personalize chemotherapy treatment for breast cancer patients. Identifying patients who will not benefit from a specific treatment means that they can be moved to a different treatment plan, and the earlier appropriate treatment is started the more likely it is that the patients will benefit from it."
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Media Contact Dr Hilary Glover Scientific Press Officer, BioMed Central Tel: +44 (0) 20 3192 2370 Mob: +44 (0) 778 698 1967 Email: hilary.glover@biomedcentral.com
Notes to Editors
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Genetic predictor of breast cancer response to chemotherapy
New under the sun: Recurrent genetic mutations in melanoma
Public release date: 9-May-2012 [ | E-mail | Share ]
Contact: Nicole Davis ndavis@broadinstitute.org 617-714-7152 Broad Institute of MIT and Harvard
Melanoma the deadliest and most aggressive form of skin cancer has long been linked to time spent in the sun. Now a team led by scientists from the Broad Institute and Dana-Farber Cancer Institute has sequenced the whole genomes of 25 metastatic melanoma tumors, confirming the role of chronic sun exposure and revealing new genetic changes important in tumor formation.
In an article published online May 9 in Nature, the authors provide the first high-resolution view of the genomic landscape of human melanoma tumors. Previous genetic analyses have focused on the exomes of many types of cancer tumors, concentrating on the tiny fraction of the genome that provides the genetic code for producing proteins. Whole genomes contain a wealth of genetic information, and by sequencing and analyzing 25 metastatic melanoma tumors a significant technical and computational feat scientists can learn vastly more about the variety of genetic alterations that matter in melanoma.
"Sequencing the whole genome certainly adds a richness of discovery that can't be fully captured with a whole exome," said Levi A. Garraway, a senior associate member of the Broad Institute, an associate professor at Dana-Farber Cancer Institute and Harvard Medical School, and co-senior author of the paper.
"By looking across the entire genome you can more accurately determine the background mutation rate and the different classes of mutations, and more confidently describe the pattern of ultraviolet-induced mutagenesis in melanoma," said Michael F. Berger, co-first author of the paper. He worked in the Broad's cancer genome analysis group and with Garraway as a research scientist and computational biologist before moving to Memorial Sloan-Kettering Cancer Center.
When the scientists explored the whole genome data generated and analyzed at the Broad, they found that the rates of genetic mutations rose along with chronic sun exposure in patients, confirming the role of sun damage in disease development.
"Whole-genome analysis of human melanoma tumors shows for the first time the existence of many structural rearrangements in this tumor type," said Lynda Chin, a senior associate member of the Broad and co-senior author of the paper. Formerly at Dana-Farber and Harvard Medical School, she is now chair of the Department of Genomic Medicine at the University of Texas MD Anderson Cancer Center.
As expected, the scientists detected known BRAF and NRAS mutations in 24 of the 25 tumors. Both genes are involved in sending signals important in cell growth.
One other gene leaped out: PREX2, previously implicated in breast cancer for blocking a tumor-suppressor pathway, was altered in 44 percent of patients. In a larger validation cohort of 107 tumors, the frequency of the mutation was 14 percent.
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New under the sun: Recurrent genetic mutations in melanoma
Why Seattle Genetics Shares Dropped Then Rallied
By Sean Williams | More Articles May 9, 2012 |
Although we don't believe in timing the market or panicking over market movements, we do like to keep an eye on big changes -- just in case they're material to our investing thesis.
What: Shares of biotech company Seattle Genetics (Nasdaq: SGEN) have had a wild ride this morning following its first-quarter earnings results. After being down 10% early in the trading session, shares are up more than 2% as of this writing.
So what: For the quarter, Seattle Genetics reported a near-quadrupling in sales to $48.2 million as the company sold $34.5 million worth of its cancer drug Adcetris, which was approved by the Food and Drug Administration in August for the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Its quarterly loss came in at $0.11 per share. Although the loss met Wall Street's estimates, sales estimates for Adcetris fell about $3 million shy of the consensus. For the year, Seattle Genetics forecast Adcetris sales of $140 million-$150 million and collaboration/licensing revenue of $55 million-$65 million.
Now what: Despite the sales miss, RBC Capital told investors this morning that any dip in Seattle Genetics shares is a buying opportunity, as it expects the company to report positive data at the ASCO conference. That may be partly responsible for the strength in its share price since it opened significantly lower this morning. As for me, I see Seattle Genetics as largely range-bound until it can produce that elusive quarterly profit.
Craving more input? Start by adding Seattle Genetics to your free and personalized watchlist so you can keep up on the latest news with the company.
Response Genetics, Inc. Announces First Quarter Financial Results
LOS ANGELES--(BUSINESS WIRE)--
Response Genetics Inc. (Nasdaq:RGDX - News), (the Company), a company focused on the development and sale of molecular diagnostic tests for cancer, today announced its consolidated financial results for the first quarter ended March 31, 2012.
Total revenues for the quarter ended March 31, 2012 were $4.0 million, compared to $5.9 million for the quarter ended March 31, 2011 was largely as a result of the expected decrease in pharmaceutical client revenue. The Companys ResponseDX revenue decreased slightly to $3.0 million for the quarter ended March 31, 2012, compared to $3.1 million for the quarter ended March 31, 2011.
The Companys first quarter 2012 net loss increased compared to the first quarter of 2011, while the sequential net loss decreased for the quarter ended March 31, 2012. Net loss for the quarter ended March 31, 2012 was $3.1 million, compared with a net loss of $0.3 million for the quarter ended March 31, 2011 and net loss of $3.9 million for the quarter ended December 31, 2011.
Cash and cash equivalents at March 31, 2012, were $5.7 million, compared to $1.7 million at December 31, 2011.
In the first quarter of 2012 we accomplished what needed to be done first we strengthened our balance sheet when we raised $7.8 million of cash, said Thomas Bologna, the Companys recently appointed Chairman & Chief Executive Officer. We also began implementing programs to put our company on the right track and took action to recover from the transition that the Company faced in 201l. While we appreciate that it will take time to achieve the results that we fully expect to deliver to our shareholders, we believe we are making good progress on what needs to be done and putting the team in place to make it happen. We believe our company is in the right space and we have the foundation and wherewithal to capitalize on our strengths and the opportunities in front of us.
Excluding cost of revenue, total operating expenses for the first quarter were $4.4 million, compared to $3.5 million for the same period last year. The increase in total operating expenses of $0.9 million was due to an increase in general and administrative expenses of $0.5 million and research and development expenses of $0.4 million.
The increase in general and administrative expenses was a result of an increase of $0.2 million in stock based compensation expense, $0.1 million in bad debt expense, $0.1 million in consulting expense, $0.1 million of equipment/maintenance expense and $0.1 million in legal fees, offset by a decrease in business tax of $0.1 million.
The increase in research and development expenses was due to an increase in personnel expenses and associated laboratory supplies and reagents related to increased research and development activity.
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Response Genetics, Inc. Announces First Quarter Financial Results
Seattle Genetics Announces Data from Investigator Trial of ADCETRIS™ in Relapsed Cutaneous T-Cell Lymphoma
BOTHELL, Wash.--(BUSINESS WIRE)--
Seattle Genetics, Inc. (Nasdaq: SGEN - News) today announced that interim results from an investigator-sponsored phase II clinical trial of ADCETRIS (brentuximab vedotin) in patients with relapsed cutaneous T-cell lymphoma (CTCL) were presented at the Society for Investigative Dermatology annual meeting being held May 9-12, 2012 in Raleigh, NC. ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30. ADCETRIS has not been approved for use in CTCL.
The trial enrolled CTCL patients with mycosis fungoides (MF) or Sezary syndrome. At the time of data analysis, 17 patients had been enrolled, including 16 with MF and one with Sezary syndrome. Patients had received a median of six prior therapies, including a median of four prior systemic therapies. The primary endpoint of the trial is clinical response rate. Secondary endpoints include correlation of clinical response with CD30 expression levels, duration of response, progression-free survival and safety. The study is led by principal investigator Dr. Youn H. Kim, Professor, Department of Dermatology, and Director, Multidisciplinary Cutaneous Lymphoma Program at Stanford University School of Medicine in Stanford, CA. Key findings include:
This is the second data set reported with ADCETRIS in CTCL patients. At the T-Cell Lymphoma Forum in January 2012, interim data were presented from a phase II investigator-sponsored trial in CD30-positive CTCL patients, including lymphomatoid papulosis, primary cutaneous anaplastic large cell lymphoma (pcALCL) or MF. In the trial, which is being conducted by Dr. Madeleine Duvic at The University of Texas MD Anderson Cancer Center, 11 of 17 evaluable patients (65 percent) achieved an objective response, including seven complete remissions (CRs) and four partial remissions (PRs). The most common adverse events were Grade 1, including diarrhea, chest tightness, alopecia, nausea, elevated liver enzymes and peripheral neuropathy.
Seattle Genetics and Millennium: The Takeda Oncology Company recently initiated a randomized phase III clinical trial of ADCETRIS for relapsed CD30-positive CTCL patients. The trial will assess ADCETRIS versus investigators choice of methotrexate or bexarotene in patients with CD30-positive CTCL, including those with pcALCL or MF. The primary endpoint of the study is overall response rate lasting at least 4 months. Approximately 124 patients will be enrolled in the pivotal trial. The phase III trial is being conducted under a Special Protocol Assessment agreement from the U.S. Food and Drug Administration (FDA). The study also received European Medicines Agency scientific advice.
About CTCL
Lymphoma is a general term for a group of cancers that originate in the lymphatic system. There are two major categories of lymphoma: Hodgkin lymphoma and non-Hodgkin lymphoma. Cutaneous lymphomas are a category of non-Hodgkin lymphomas that primarily involve the skin. According to the Cutaneous Lymphoma Foundation, CTCL is the most common type of cutaneous lymphoma and typically presents with red, scaly patches or thickened plaques of skin that often mimic eczema or chronic dermatitis. Progression from limited skin involvement is variable and may be accompanied by tumor formation, ulceration and exfoliation, complicated by itching and infections. Advanced stages are defined by involvement of lymph nodes, peripheral blood and internal organs. According to published literature, up to 50 percent of CTCL patients lesions express CD30.
About ADCETRIS
ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.
ADCETRIS (brentuximab vedotin) received accelerated approval from the U.S. Food and Drug Administration for two indications: (1) the treatment of patients with Hodgkin lymphoma after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates, and (2) the treatment of patients with systemic anaplastic large cell lymphoma (sALCL) after failure of at least one prior multi-agent chemotherapy regimen. The indications for ADCETRIS are based on response rate. There are no data available demonstrating improvement in patient-reported outcomes or survival with ADCETRIS.
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Seattle Genetics Announces Data from Investigator Trial of ADCETRIS™ in Relapsed Cutaneous T-Cell Lymphoma
NewLink Genetics Corporation Reports First Quarter 2012 Financial Results
AMES, Iowa, May 10, 2012 (GLOBE NEWSWIRE) -- NewLink Genetics Corporation (Nasdaq:NLNK - News), a biopharmaceutical company focused on discovering, developing and commercializing cancer therapeutics, today reported consolidated financial results for the first quarter of 2012, and provided an update on the progress of its clinical development programs.
"During the first quarter of 2012 we continued to advance our pivotal trial in pancreatic cancer and are also moving forward on a number of other HyperAcute immunotherapy development programs including those to treat melanoma and lung and kidney cancers," commented Dr. Charles Link, Chairman and Chief Executive Officer of NewLink. "We also made strides in our IDO pathway inhibitor program and are looking forward to presenting new data for a number of these programs at both DDW and ASCO. We believe that the receipt of patent allowances in both of our core programs will also facilitate our business development activities."
First quarter 2012 Financial Results
Financial Guidance
NewLink is maintaining its financial guidance and continues to expect to end 2012 with about $20 million in cash, cash equivalents and marketable securities. NewLink continues to anticipate that this capital should allow it to fund its operations through 2013 based on its current operating plans.
2012 Key Accomplishments to Date
Upcoming Activities
NewLink expects to present at the following investor conferences:
NewLink expects to present at the following oncology and pharmacology meetings:
About NewLink Genetics Corporation
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NewLink Genetics Corporation Reports First Quarter 2012 Financial Results
Seattle Genetics to Present at Bank of America Merrill Lynch Health Care Conference
BOTHELL, Wash.--(BUSINESS WIRE)--
Seattle Genetics, Inc. (NASDAQ:SGEN - News) announced today that management will present at the Bank of America Merrill Lynch 2012 Health Care Conference on Tuesday, May 15, 2012 at 1:00 p.m. Pacific Time. The presentation will be webcast live and available for replay from Seattle Genetics website at http://www.seattlegenetics.com in the Investors and News section.
About Seattle Genetics
Seattle Genetics is a biotechnology company focused on the development and commercialization of monoclonal antibody-based therapies for the treatment of cancer. The U.S. Food and Drug Administration granted accelerated approval of ADCETRIS in August 2011 for two indications. ADCETRIS is being developed in collaboration with Millennium: The Takeda Oncology Company. In addition, Seattle Genetics has three other clinical-stage antibody-drug conjugate (ADC) programs: SGN-75, ASG-5ME and ASG-22ME. Seattle Genetics has collaborations for its ADC technology with a number of leading biotechnology and pharmaceutical companies, including Abbott, Bayer, Celldex Therapeutics, Daiichi Sankyo, Genentech, GlaxoSmithKline, Millennium, Pfizer and Progenics, as well as ADC co-development agreements with Agensys, an affiliate of Astellas, and Genmab. More information can be found at http://www.seattlegenetics.com.
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Seattle Genetics to Present at Bank of America Merrill Lynch Health Care Conference
Interleukin Genetics Reports First Quarter 2012 Financial Results
WALTHAM, Mass.--(BUSINESS WIRE)--
Interleukin Genetics,Inc. (OTCQB: ILIU.PK - News) today announced financial and operational results for the first quarter ended March 31, 2012.
Total revenue for the three months ended March 31, 2012 was $678,000, compared to $719,000 for the same period in the prior year. The decrease was attributable to lower genetic test revenue.
Research and development expenses were $446,000 for the three months ended March 31, 2012, compared to $305,000 for the same period in the prior year. The Company continues its work in its weight management and periodontal disease programs.
Selling, general, and administrative expenses were $1.1 million for the three months ended March 31, 2012, compared to $1.2 million for the same period in the prior year. The decrease was primarily attributable to decreased corporate professional fees and patent-related legal fees offset in part by increased compensation, consulting and sales commissions paid to Amway.
The Company reported a net loss of $1.4 million, or $(0.04) per basic and diluted common share, for the first quarter of 2012, compared to a loss of $1.3 million, or $(0.03) per basic and diluted share, for the same period in the prior year. On March 31, 2012, the Company had cash and cash equivalents of $732,000 and had $1.3 million available under its credit facility with Pyxis Innovations, Inc.
The Company expects that its current and anticipated financial resources, including the $1.3 million available as of March 31, 2012 under the credit facility, which was borrowed on April 13, 2012, are adequate to maintain current and planned operations at least through June 30, 2012. The Companys independent registered public accounting firm has included an explanatory paragraph in their opinion in connection with the 2011 audit, relating to the Company's ability to continue as a going concern.
While recognized genetic test revenue this quarter was lower than last years for this corresponding quarter, our deferred revenue increased by over 35% or more than $300,000 in this quarter indicating that unit test sales are continuing to grow nicely, said Lewis H. Bender, Chief Executive Officer of Interleukin Genetics. In addition, enrollment in our clinical study in collaboration with Renaissance Health and the University of Michigan to demonstrate the utility of using our PST genetic test in the management of dental patients was completed and we successfully delivered 5,186 genotypes to the University thereby completing our portion of the program.
Conference Call and Webcast Information
Interleukin Genetics will host a live conference call and webcast today at 4:30 p.m. EDT to review the Companys new business developments and first quarter financial results. To access the live call, dial 877-324-1976 (domestic) or 631-291-4550 (international). The live webcast and replay access will be available on the Investors section of the Companys Website at: http://www.ilgenetics.com.
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Interleukin Genetics Reports First Quarter 2012 Financial Results
Penn researchers report a gene-therapy success
The study involved painstaking molecular analysis of blood samples taken annually from the patients, who participated in separate studies begun in 2000, 2002, and 2004.
"We were astonished that we could detect the modified cells for so long. It's a relatively small number of patients, but more than 500 years of patient data," said University of Pennsylvania pathologist Bruce Levine, a leader of the research. "But it's difficult to separate with certainty the effectiveness of this treatment from the antiretrovirals."
Gene therapy harnesses the insidious ability of viruses to slip their DNA into the cells they infect. By neutralizing a virus and then using it as a "vector" to insert DNA that is helpful rather than harmful, gene therapy can theoretically treat ailments ranging from arthritis to infections and cancer.
Levine, his Penn colleague Carl June, and their team have tested a variety of ways to outwit HIV with gene therapy. Their approach has focused on T cells, which are the big guns of the immune system but also the cells that HIV infects. The researchers took some of the patients' T cells and inserted a gene that makes them better at recognizing and killing HIV-infected cells. Then these super-T cells were multiplied using growth-stimulation technology and put back into the patient.
Over the years, many other research groups have tried using modified T cells, but the patient's immune system perceived them as invaders and wiped them out, sometimes within hours.
TiGenix : Presenting at Key Conferences – Spring 2012
LEUVEN, BELGIUM--(Marketwire -05/08/12)- TiGenix (TIG), a leader in the field of cell therapy, announced today that during the months of May and June the company will present at a number of key events in Europe and the U.S. geared at investor, industry, and academic audiences to highlight the commercial potential of ChondroCelect, the only approved cell therapy in Europe, and of the company's innovative proprietary allogeneic stem cell platform with programs in Phase I, II, and III for a range of inflammatory and autoimmune diseases.
May 15-16 BioEquity, Marriott Hotel, Frankfurt, Germany Presenter: Eduardo Bravo, CEO Date & time: Tuesday, May 15, 16:00-16:25 Room: Level 1, Room Gold 1
May 21-23 World Stem Cells and Regenerative Medicine Congress, Victoria Park Plaza, London, UK Presenter: Eduardo Bravo, CEO Date & time: Monday, May 21, 15:25 -15:50 Title: Cell Therapy & Regenerative Medicine - Progressing into phase III with an orphan indication
May 24 Knowledge for Growth, ICC Ghent, Belgium Presenter: Eduardo Bravo, CEO Time: 11:30 Keynote speech - Advanced therapies: this time it is for real
June 5-8 18th International Stem Cell Therapy Sociey Annual Meeting, Sheraton Seattle, WA, U.S. Presenter: Eduardo Bravo, CEO Date & time: June 7, 13:45-15:15 Title: Plenary Session 4 - Regenerative Medicine and Positioning for Commercial Success - Lessons from the commercial roll out of ChondroCelect in Europe
June 18-21 BIO International Convention, Boston Convention & Exhibition Center, MA, U.S. Presenter: Eduardo Bravo, CEO Date & time: June 20, 15:00-15:45 Title: Stem Cell Therapies...Fact or Fiction?
June 23 VFB Biotech Congres, Leuven, Belgium Location: Imec, Kapeldreef 75, Leuven Presenter: Gil Beyen, Chief Business Officer Time: 11am
June 23 Dag van de Biotechnologie, Leuven, Belgium Location: TiGenix headquarters, Leuven Event: Open day event throughout Flanders for all biotech companies & academic labs Time: 10am-5pm
About TiGenixTiGenix NV (TIG) is a leading European cell therapy company with a marketed product for cartilage repair, ChondroCelect, and a strong pipeline with clinical stage allogeneic adult stem cell programs for the treatment of autoimmune and inflammatory diseases. TiGenix is based out of Leuven (Belgium) and has operations in Madrid (Spain), and Sittard-Geleen (the Netherlands). For more information please visit http://www.tigenix.com.
Forward-looking information This document may contain forward-looking statements and estimates with respect to the anticipated future performance of TiGenix and the market in which it operates. Certain of these statements, forecasts and estimates can be recognised by the use of words such as, without limitation, "believes", "anticipates", "expects", "intends", "plans", "seeks", "estimates", "may", "will" and "continue" and similar expressions. They include all matters that are not historical facts. Such statements, forecasts and estimates are based on various assumptions and assessments of known and unknown risks, uncertainties and other factors, which were deemed reasonable when made but may or may not prove to be correct. Actual events are difficult to predict and may depend upon factors that are beyond TiGenix' control. Therefore, actual results, the financial condition, performance or achievements of TiGenix, or industry results, may turn out to be materially different from any future results, performance or achievements expressed or implied by such statements, forecasts and estimates. Given these uncertainties, no representations are made as to the accuracy or fairness of such forward-looking statements, forecasts and estimates. Furthermore, forward-looking statements, forecasts and estimates only speak as of the date of the publication of this document. TiGenix disclaims any obligation to update any such forward-looking statement, forecast or estimates to reflect any change in TiGenix' expectations with regard thereto, or any change in events, conditions or circumstances on which any such statement, forecast or estimate is based, except to the extent required by Belgian law.
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TiGenix : Presenting at Key Conferences - Spring 2012
Nuvilex Announces Excitement Grows in Japan over Encapsulated Living Cell Technology Oncological Applications
SILVER SPRING, Md.--(BUSINESS WIRE)--
Nuvilex, Inc. (OTCQB:NVLX), an emerging biotechnology provider of cell and gene therapy solutions, reports the Chairman of its associate company, SG Austria, Dr. Walter Gunzburg, participated in multiple private meetings with leading Japanese biotech and pharmaceutical companies following the recent Annual Meeting of the Organisation for Oncology and Translational Research (OOTR), where he was a invited guest speaker.
The meetings took place immediately after his recent bench to bedside presentation of data from the clinical trials for the treatment of solid tumors using the companys cutting-edge living cell encapsulation technology. Nuvilex and SG Austria have been actively working to advance the value and use of the live cell encapsulation technology throughout North America and Europe, and are encouraged by the positive response in the Asia-Pacific Rim. Drs. Gunzburg and Salmons have been increasing the number of companies that know about this cutting-edge live cell encapsulation technology and their efforts have been paying off in terms of invitations for in-depth company meetings.
Dr. Robert Ryan, Chief Executive Officer of Nuvilex, commented, Japan is well known as an important producer and consumer of advanced medical products and were excited to report there was keen interest in the use of live cell encapsulation. In addition, we are noting the living cell encapsulation technology is proving to be of great interest to a number of biotech companies developing cell therapies for the treatment of a wide variety of diseases.
About Nuvilex
Nuvilex, Inc. (OTCQB:NVLX) is an emerging international biotechnology provider of live therapeutically valuable, encapsulated cells and services for research and medicine. Through substantial effort, aspects of our corporate activities alone and in concert with SG Austria are nearing completion, ultimately providing for a strong future together. Our companys clinical offerings will include cancer, diabetes and other treatments using the companys industry-leading cell and gene therapy expertise and cutting edge, live-cell encapsulation technology.
Safe Harbor Statement
This press release contains forward-looking statements described within the 1995 Private Securities Litigation Reform Act involving risks and uncertainties including product demand, market competition, and meeting current or future plans which may cause actual results, events, and performances, expressed or implied, to vary and/or differ from those contemplated or predicted. Investors should study and understand all risks before making an investment decision. Readers are recommended not to place undue reliance on forward-looking statements or information. Nuvilex is not obliged to publicly release revisions to any forward-looking statement, reflect events or circumstances afterward, or disclose unanticipated occurrences, except as required under applicable laws.
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Nuvilex Announces Excitement Grows in Japan over Encapsulated Living Cell Technology Oncological Applications
Errors of The Human Body – Official Trailer – Video
07-05-2012 10:59 Here it is. The First Trailer for the Scientific Thriller Errors of The Human Body. Currently still seeking funds for post production through crowdfunding at
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Errors of The Human Body - Official Trailer - Video
Dorothy Roberts: Race and the New Biocitizen- Tarrytown 2010 – Video
07-05-2012 15:13 Dorothy Roberts, Professor at Northwestern University, discusses how emerging biotechnologies are reconfiguring, reforming and revising notions of race in potentially dangerous ways at the 2010 Tarrytown Meeting. The Tarrytown Meetings bring together people working to ensure that human biotechnologies and related emerging technologies support rather than undermine social justice, equality, human rights, ecological integrity and the common good. Find out more about the Tarrytown Meetings here: To find more videos, check out the Tarrytown Youtube channel: Presentation Excerpt: The expansion of genetic research and technologies has helped us cross a threshold into a new type of biopolitics concerned with our capacity to control and manipulate human life. As British sociologist Nicholas Rose has shown, so-called biological citizenship is grounded in the unprecedented authority wielded by individuals over their well-being at the molecular level. According to Rose, "our very biological life itself has entered the domain of decision and choice." Biological citizenship entails both individuals' autonomy over personal welfare and a biosociality that links people together around their common genetic traits. Genetic information enables individuals not only to manage their own health, but also to unite with others around their common health conditions, as revealed by DNA testing. Rose and others celebrate biocitizenship because it enhances ...
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Dorothy Roberts: Race and the New Biocitizen- Tarrytown 2010 - Video
Advancing Genomics into Personalized Medicine – Video
07-05-2012 15:22 High-throughput technology and the data it generates is evolving and advancing basic science into clinical science and personalized medicine. But while currently available methods exist to rapidly and efficiently produce DNA, epigenetic, and RNA whole-genome profiles from individual tissue samples and cell lines, data analysis and deconvolution remain challenging. To address this issue, methods of knowledge-based functional analysis such as ontology enrichment, interactome, and causal networks have been developed. These analyses rely on databases designed to accommodate complex aspects of mammalian functionality, for example, coordinated expression of multiple genes to effect a single function, RNA splice variants, or protein isoforms. Webinar participants will discuss knowledge-based analytical methods, and how they can be used for functional analysis of OMICs datasets by cheminformatics and bioinformatics software tools such as network-generation algorithms, ontology enrichment, interactome calculations, and pathway modeling. The application of these analytical methods to advances in understanding breast tumor heterogeneity and the potential development of a targeted therapy based on this knowledge will also be discussed.
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Advancing Genomics into Personalized Medicine - Video
Researchers discover gene that leads to severe weight gain with antipsychotic treatment
Public release date: 7-May-2012 [ | E-mail | Share ]
Contact: Emily Ng eng3@nshs.edu 516-562-2670 North Shore-Long Island Jewish (LIJ) Health System
Antipsychotic medications are increasingly prescribed in the US, but they can cause serious side effects including rapid weight gain, especially in children. In the first study of its kind, researchers at Zucker Hillside Hospital and the Feinstein Institute for Medical Research identified a gene that increases weight gain in those treated with commonly-used antipsychotic drugs. These findings were published in the May issue of Archives of General Psychiatry.
Second-generation antipsychotics (SGAs) were used as the treatment in this study. SGAs are commonly used to treat many psychotic and nonpsychotic disorders. However, it is important to note that these SGAs are associated with substantial weight gain, including the development of obesity and other cardiovascular risk factors. The weight gain side effect of SGAs is significant because it often results in a reduced life expectancy of up to 30 years in those who suffer from chronic and severe mental illnesses. The weight gain also prompts some to stop taking the medication, adversely impacting their quality of life.
In this genome-wide association study (GWAS), researchers first evaluated a group of pediatric patients in the US being treated for the first time with antipsychotics. They then replicated the result in three independent groups of patients who were in psychiatric hospitals in the United States and Germany or participating in European antipsychotic drug trials. The gene that was identified to increase weight gain, MC4R or melanocortin 4 receptor, has been previously identified as being linked to obesity and type 2 diabetes. In the new study, it was found that patients gained up to 20 pounds when on treatment.
"This study offers the prospect of being able to identify individuals who are at greatest risk for severe weight gain following antipsychotic treatment," said Anil Malhotra, MD, investigator at the Zucker Hillside Hospital Department of Psychiatry Research and Feinstein Institute for Medical Research. "We hope that those who are at risk could receive more intensive or alternative treatment that would reduce the potential for weight gain and we are currently conducting studies to identify such treatment."
Additional Details About the Study
Researchers conducted the first GWAS of SGA-induced weight gain in patients carefully monitored for medication adherence who were undergoing initial treatment with SGAs. To confirm results, they next assessed three independent replication cohorts: 1) a cohort of adult subjects undergoing their first treatment with a single SGA (clozapine), 2) a cohort of adult subjects treated with the same SGAs as in our discovery sample, and 3) a cohort of adult subjects in the first episode of schizophrenia and enrolled in a randomized clinical trial of antipsychotic drugs.
The discovery cohort consisted of 139 pediatric patients undergoing first exposure to SGAs. The 3 additional cohorts consisted of 73, 40, and 92 subjects. Patients in the discovery cohort were treated with SGAs for 12 weeks. Additional cohorts were treated for 6 and 12 weeks.
This GWAS yielded 20 single-nucleotide polymorphisms at a single locus exceeding a statistical threshold of P10-5. This locus, near the melanocortin 4 receptor (MC4R) gene, overlaps a region previously identified by large-scale GWAS of obesity in the general population. Effects were recessive, with minor allele homozygotes gaining extreme amounts of weight during the 12-week trial. These results were replicated in 3 additional cohorts, with rs489693 demonstrating consistent recessive effects; meta-analysis revealed a genome-wide significant effect. Moreover, consistent effects on related metabolic indices, including triglyceride, leptin, and insulin levels were observed.
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Researchers discover gene that leads to severe weight gain with antipsychotic treatment
Gene that leads to severe weight gain with antipsychotic treatment discovered
ScienceDaily (May 7, 2012) Antipsychotic medications are increasingly prescribed in the US, but they can cause serious side effects including rapid weight gain, especially in children. In the first study of its kind, researchers at Zucker Hillside Hospital and the Feinstein Institute for Medical Research identified a gene that increases weight gain in those treated with commonly-used antipsychotic drugs.
These findings were published in the May issue of Archives of General Psychiatry.
Second-generation antipsychotics (SGAs) were used as the treatment in this study. SGAs are commonly used to treat many psychotic and nonpsychotic disorders. However, it is important to note that these SGAs are associated with substantial weight gain, including the development of obesity and other cardiovascular risk factors. The weight gain side effect of SGAs is significant because it often results in a reduced life expectancy of up to 30 years in those who suffer from chronic and severe mental illnesses. The weight gain also prompts some to stop taking the medication, adversely impacting their quality of life.
In this genome-wide association study (GWAS), researchers first evaluated a group of pediatric patients in the US being treated for the first time with antipsychotics. They then replicated the result in three independent groups of patients who were in psychiatric hospitals in the United States and Germany or participating in European antipsychotic drug trials. The gene that was identified to increase weight gain, MC4R or melanocortin 4 receptor, has been previously identified as being linked to obesity and type 2 diabetes. In the new study, it was found that patients gained up to 20 pounds when on treatment.
"This study offers the prospect of being able to identify individuals who are at greatest risk for severe weight gain following antipsychotic treatment," said Anil Malhotra, MD, investigator at the Zucker Hillside Hospital Department of Psychiatry Research and Feinstein Institute for Medical Research. "We hope that those who are at risk could receive more intensive or alternative treatment that would reduce the potential for weight gain and we are currently conducting studies to identify such treatment."
Additional Details About the Study
Researchers conducted the first GWAS of SGA-induced weight gain in patients carefully monitored for medication adherence who were undergoing initial treatment with SGAs. To confirm results, they next assessed three independent replication cohorts: 1) a cohort of adult subjects undergoing their first treatment with a single SGA (clozapine), 2) a cohort of adult subjects treated with the same SGAs as in our discovery sample, and 3) a cohort of adult subjects in the first episode of schizophrenia and enrolled in a randomized clinical trial of antipsychotic drugs. The discovery cohort consisted of 139 pediatric patients undergoing first exposure to SGAs. The 3 additional cohorts consisted of 73, 40, and 92 subjects. Patients in the discovery cohort were treated with SGAs for 12 weeks. Additional cohorts were treated for 6 and 12 weeks.
This GWAS yielded 20 single-nucleotide polymorphisms at a single locus exceeding a statistical threshold of P10-5. This locus, near the melanocortin 4 receptor (MC4R) gene, overlaps a region previously identified by large-scale GWAS of obesity in the general population. Effects were recessive, with minor allele homozygotes gaining extreme amounts of weight during the 12-week trial. These results were replicated in 3 additional cohorts, with rs489693 demonstrating consistent recessive effects; meta-analysis revealed a genome-wide significant effect. Moreover, consistent effects on related metabolic indices, including triglyceride, leptin, and insulin levels were observed.
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Gene that leads to severe weight gain with antipsychotic treatment discovered
New Tanenbaum Centre for Pharmacogenetics to accelerate gene-based personalized medicine in psychiatry
$19 million collaboration fuelling groundbreaking discoveries
TORONTO, May 7, 2012 /CNW/ - Lawrence Tanenbaum, O.C., along with his wife Judy Tanenbaum, today joined the Honourable Brad Duguid Minister of Economic Development and Innovation, renowned researcher Dr. Jim Kennedy and Dr. Catherine Zahn, President and CEO, CAMH, to announce a $19 million collaboration and open the Tanenbaum Centre for Pharmacogenetics at the Centre for Addiction and Mental Health (CAMH).
This centre, a collaboration between Larry Tanenbaum, the Ontario Government and CAMH, has been established to support the groundbreaking research in the DNA laboratory of Dr. Kennedy and the clinic of Dr. Daniel Mueller to accelerate the time it takes to get genetic information to physicians and patients across Ontario. The Centre will be part of the Campbell Family Mental Health Research Institute at CAMH's College Street location.
"Pharmacogenetics" is an aspect of personalized medicine research that aims to help doctors understand in advance which individuals carry a genetic risk for serious side-effects from specific drugs. Genetic testing will also be helpful in determining who is more likely to respond to a given medication and if dose adjustments need to be considered. Similar work is being done in cancer and pain management, but CAMH is one of the world leaders in psychiatric applications of this research.
"Mistakes in drug treatment can result in devastating, even tragic side-effects. Still, inaccurate predictions of treatment for depression happen in about 30 per cent of cases and 11 per cent of all mental health patients are at serious genetic risk of suffering from inappropriate dosages of medication. The size of the problem is staggering, but the research in gene science that Dr. Kennedy and his team are doing can - and will - change that," said Mr. Tanenbaum, Chairman and CEO of the Kilmer Group, Chair of the Board, Maple Leaf Sports and Entertainment, and Governor of the NHL, NBA and Major League Soccer.
"We are honoured to be part of this collaboration because it holds the promise that one day soon drugs will be adapted to each person's genetic make-up. The faster these discoveries can get out of the lab, the sooner more effective and safe therapies will become available - changing and saving lives."
"Ontario's ongoing commitment to world-class research is one reason the province is home to more than 500 top neuroscientists," said Minister of Economic Development and Innovation Brad Duguid. "Our support of the new Tanenbaum Centre for Pharmacogenetics promises to improve medical care and quality of life for psychiatric patients and their families, save our health care system millions of dollars, while creating good jobs."
Most recently, Dr. Kennedy's lab has identified a new genetic risk factor for serious weight gain, a side-effect for 40 per cent of schizophrenia patients who receive a commonly used group of anti-psychotic drugs. Understanding in advance which individuals carry this genetic risk would help doctors know when to prescribe different drugs.
Along with establishing the Centre, the investment will move this and other genetic tests into medical practice through "lab-on-a-chip" technology currently in development. Clinical delivery of these tests is already available for CAMH patients, and extension to GTA-area physicians is expected to begin in 2014. Furthermore, the biotechnology development initiative within this program will create an increasing number of knowledge-based jobs in Ontario as the core genetics research expands.
For Dr. Kennedy, this investment sets in motion the potential to revolutionize psychiatry by scaling up testing and fueling the drive to find new genetic tests: "If we could prevent serious side effects such as movement disorders, sleep disturbance and increased risk of cardiovascular disease, I truly believe more people in need would stay on their medication and derive the long-term benefits of better mental health, living longer more productive and fuller lives with their families."
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New Tanenbaum Centre for Pharmacogenetics to accelerate gene-based personalized medicine in psychiatry
Gene technology: A new breakthrough research
Bangalore, May 8 : In technologically advanced world, there are numerous research and developments that take place to improve not only the standard of living but also to give a normal living.
One such development in the health field is the gene technology. With the advancement of this therapy, a patient is treated by its own cells, DNA, skin graft to cure the problem of the person.
Addressing a press conference here, Dr Sunita Agarwal, Medical Director, Gene Research Foundation, presented a case of city boy Naren (name changed) who was born dumb, deaf and blind from childhood due to genetic disorder.
Naren was diagnosed with the Usher's syndrome, a cognital error where he had no vision and was hearing and speech impaired. He underwent a surgery, Autologous Retinal Transplant, based on the concept of gene therapy.
The BCA graduate, however, after the therapy of three long years, has managed to get back his vision. "Since its a genetic disorder, the vision is never going to be normal like we all possess but through this therapy, we are atempting to give him a better clear vision if not in its entirety," said Dr Agarwal said.
The gene therapy is claimed to be one of its kind and it is said to be a breakthrough solution for the future of the medicinal world.
"Through this technology, diseases like blindness, diabetes, cancer, arthritis can be appreciably better within ten days of injection course," she added. (UNI)
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Gene technology: A new breakthrough research
Californian GMO labeling: What would it mean for food companies?
The Californian Right to Know campaign in support of labeling foods and ingredients produced using genetic engineering looks set for inclusion in the states November ballot, after it attracted nearly a million signatures. If enacted, what would the proposed law mean for food manufacturers?
The state has up to seven weeks to validate the 971,126 signatures. If they are validated, and voters approve the measure in November, food manufacturers could be required to label genetically modified (GM) foods and ingredients sold in California from July 1, 2014.
The California Right to Know Genetically Engineered Food Act would require such foods to be labeled in a clear and conspicuous manner, whether raw agricultural commodities or processed foods.
The bill reads that a food would deemed to be misbranded unless labeled: In the case of any processed food, in clear and conspicuous language on the front or back of the package of such food, with the words Partially Produced with Genetic Engineering or May be Partially Produced with Genetic Engineering
GMOs deemed unnatural
In addition, food labeled as natural would be deemed misbranded under the legislation if it contained genetically modified ingredients, in line with the precept of a swathe of lawsuits that have been brought against food companies in California. Currently the US Food and Drug Administration has no definition of the word natural.
The proposed legislation contains a number of exceptions, including allowances for unintentional presence of GM ingredients, and meat or milk from animals that may have eaten feed produced using genetic engineering. These would be exempt from labeling under the proposal, as is the case in European law.
Until July 2019, food products would also be exempt from labeling if a GM ingredient accounts for less than 0.5% of the foods total weight, and foods could contain up to ten such ingredients.
Industry opposition
Several major industry organizations and trade groups have set up a campaign opposing the proposition, including the California Retailers Association, Grocery Manufacturers Association, American Beverage Association, and California League of Food Processors, among others . Calling the coalition Californians Against the Costly Food Labeling Proposition, they claim that labeling GM foods and ingredients could increase food prices and mislead consumers into thinking their foods are unsafe.
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Californian GMO labeling: What would it mean for food companies?
Autism – A Functional Medicine Approach to Treatment- a webinar presented on 12-15-2010 – Video
07-05-2012 12:34 Autism, just like any chronic health condition, is the result of genetic predispositions interacting with modifiable environmental factors. The key is to identify the contributing factors in each case. Some of the common factors include nutrient insufficiencies, toxin exposure, food allergies, intestinal yeast overgrowth, infections, and more. New functional medicine laboratory tests help to tailor the treatment in each case of autistic spectrum disorder. Personalized treatment based on this type of evaluation helps many patients with autism improve to varying degrees, sometimes a great deal. By Dr. Joseph Debé, Board Certified Nutritionist • • (516) 829-1515 Register for upcoming webinars at
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Autism - A Functional Medicine Approach to Treatment- a webinar presented on 12-15-2010 - Video